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Project 1 - Loss of an RNA binding protein ELAV, leads to degeneration in photoreceptor neurons through apoptosis in Drosophila melanogaster AND Project 2 - Factors affecting regulation of AcrAB-TolC efflux system in Salmonella enterica serovar Typhimurium

Anand, Hanish (2015)
M.Res. thesis, University of Birmingham.

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Neurodegenerative disorders cost billions every year and put huge burden on the health care system of nations. Because of lack of thorough understanding of mechanisms behind these diseases, there are hardly any treatments available that increase the concerns even more. Recent evidence suggests that RNA binding proteins play major role in neurodegenerative diseases because of their ability to bind RNA targets in sequence and position dependent manner and in regulating alternative splicing. Moreover, specific tissue types along with expressing transcription factors can tailor their proteome by expressing, RNA binding proteins in tissue specific manner.

In this study we investigated the role played by ELAV, first identified member of RNA binding protein superfamily, in neurodegeneration by using model organism \(Drosophila\) \(melanogaster\). We show that loss of \(elav\) leads to degeneration of photoreceptor neurons in \(Drosophila\). Also, the degeneration of neurons occurs through apoptotic pathway. We confirmed apoptosis by expressing inhibitor of apoptosis gene \(p35\), which suppressed the degeneration of photoreceptor neurons completely. We further investigated the expression of pro-apoptotic genes and observed that \(hid\) expression is increased in dying photoreceptor neurons; this increased expression due to loss of \(elav\) may be responsible in activating the apoptotic mechanism.

Type of Work:M.Res. thesis.
Supervisor(s):Fan, Yun and Piddock, Laura
School/Faculty:Colleges (2008 onwards) > College of Life & Environmental Sciences
Department:School of Biosciences
Additional Information:

Embargo until: 01/12/2016

Subjects:RA0421 Public health. Hygiene. Preventive Medicine
RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Institution:University of Birmingham
ID Code:5666
This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.
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